Name
MILK-ALKALI SYNDROME
DESCRIPTION
DETAIL
CAUSED BY EXCESSIVE INTAKE OF CAL CARBONATE OR MILK & ALKALIES. D.D. : - ADDISON DISEASE - HYPERCALCEMIA - HYPERPARATHYROIDISM - HYPERTHYROIDISM - excessive osteolysis with malignant disease - vitamin intoxication - thyroid disease - sarcoidosis - thiazide diuretic treatmentDIAGNOSED BY EXCLUSION & PT. HISTORY * SERUM CALCIUM - HIGH ( FROM MILD TO LIFE THREATENING LEVELS) * PTH LEVELS( SHOULD BE MEASURED BEFORE STARTING TT ) - LOW * SERUM PHOSPHORUS - MAY BE ELEVATED DUE TO LOW PTH LEVEL * KIDNEY FUNCTIONS - NORMAL OR SEVERELY COMPROMISED * HYPERTHYROIDISM, ADRENAL FAILURE CAN CAUSE HIGH SERUM CALCIUM LEVELS * SERUM ALBUMIN & GLOBULIN LEVELS TO CALCULATE SERUM CALCIUM LEVELS( CORRECTED ). * SERUM VIT D LEVELS - TO RULE OUT VIT D TOXICITY
TYPENOTES
RISK FACTORS: Peptic ulcer, Hiatal hernia, MalignanciesMedical Care " Mild hypercalcemia " o The only care required is discontinuation of calcium carbonate or lowering the dose to no more than 1200-1500 mg of elemental calcium a day. o In most patients, calcium supplementation should be changed to a form of calcium other than calcium carbonate. Thus, absorbable alkali is avoided. " Severe hypercalcemia " o The patient should be admitted to the hospital. o A saline diuresis, produced by infusion of large volumes of intravenous isotonic sodium chloride solution, is the treatment of choice. o Further calciuresis can be induced by treatment with intravenous loop diuretics. o The typical patient is volume depleted; therefore, volume should be replaced with saline prior to institution of diuretic therapy. Care should be taken to not induce volume depletion with the diuretics because this may worsen the hypercalcemia. o Calcium carbonate should be stopped to resolve the pathophysiology that produced the hypercalcemia. o As stated above, patients with milk-alkali syndrome may become transiently hypocalcemic during treatment with intravenous saline and intravenous diuretics. o Because laboratory studies such as PTH measurements will not have returned to normal when therapy is instituted, the serum calcium level must be monitored closely. o Pamidronate has been used successfully in the treatment of hypercalcemia secondary to milk-alkali syndrome. However, treatment of milk-alkali syndrome with bisphosphonates was associated with hypocalcemia in one series, where 6 of 11 patients with milk-alkali syndrome had treatment-induced hypocalcemia. Five of these 6 patients received bisphosphonates. Diet " A low-calcium and low-phosphorus diet is required during hypercalcemia. Activity " No activity restrictions are necessary. DRUG TREATMENT : The primary therapy of hypercalcemia in milk-alkali syndrome is intravenous volume replacement with isotonic sodium chloride solution. When ingestion of calcium carbonate has stopped, the pathophysiologic stimulus for hypercalcemia is no longer present. Hypercalcemia in this setting usually is rapidly corrected. Loss of calcium from urine can be increased with the use of a loop diuretic, but this therapy cannot be started until intravascular volume has been replenished. Renal dialysis has been used in a few patients, as has intravenous infusion of pamidronate. 1. DIURETICS : - FRUSEMIDE 2. BONE RESORPTION INHIBITORS ( ANTIRESORPTIVE ) : - PAMIDRONATE ALTERNATIVE DRUGS Disodium phosphate and monopotassium phosphate. HAZARDOUS - should be used only by experienced nephrologist and only if dialysis is unavailable PATIENT MONITORING β’ Kidney function β’ Fluid intake and output β’ Urine electrolytes PREVENTION/AVOIDANCE Avoid excess milk and/or absorbable antacids POSSIBLE COMPLICATIONS β’ Renal failure β’ Nephrocalcinosis EXPECTED COURSE/PROGNOSIS Favorable with appropriate therapy
RELATED DISEASE
Not Available Disease
DISEASE
INVESTIGATION
SERUM CREATININE, SERUM ALBUMIN, SERUM CALCIUM, URINE ROUTINE, T3, T4, TSH, COMPLETE BLOOD COUNT, PARATHYROID HORMONE ASSAY, SERUM PHOSPHORUS, SERUM GLOBULIN